The role of prostaglandins in the bronchoconstriction induced by pulmonary micro‐embolism in the guinea‐pig.

Abstract

SUMMARY1. Respiratory resistance was measured by a forced oscillation technique in vagotomized guinea-pigs before and after pulmonary micro-embolism produced by i.v. injection of 0 5 ml./kg of 10 % w/v BaSO4. Changes in quasi-static inspiratory compliance and arterial platelet count were also measured.2. Micro-embolic challenge with BaSO4 increased respiratory resistance by 27 %; this was abolished by prior treatment with indomethacin; no change in the control resistance occurred after indomethacin.3. No change in respiratory compliance or arterial platelet numbers were observed following low dose BaSO4 micro-embolism. This suggests that pulmonary microembolism produced a decrease in medium or large airway calibre, which was mediated by a prostaglandin-like substance from lung tissue, and did not require the presence of the vagus nerves.

The role of platelets in the reflex tachypnoeic response to miliary pulmonary embolism in anaesthetized rabbits

“…This could be due to inhibition of either the platelet-release reaction (Cade, 1975;Vaage, 1976) or the release of prostaglandins from lung tissue (Clay & Hughes, 1980). The data from the present experiments support the former hypothesis, i.e.…”

“…Thus, injections of autologous thromboemboli into rabbits (Thomas & Gurewich, 1965;Gurewich, Cohen & Thomas, 1968) and of barium sulphate into cats (B0, Hognestad & Vaage, 1974) resulted in a fall in the circulating platelet count and electron micrographs revealed accretions of platelets upon the surfaces of both types of emboli (Thomas, Gurewich & Ashford, 1966;B0 et al 1974). Clay & Hughes (1980) were unable to confirm platelet activation by barium sulphate but this report is unique. Platelets will adhere to the embolic material used in our experiments because platelet adhesion to glass beads is a standard test of platelet function (Hellem, 1960).…”

“…Certain non-steroidal anti-inflammatory drugs (NSAIDs), which are potent inhibitors of the platelet-release reaction (Zucker & Peterson, 1968), have been shown to prevent both the vasomotor (Cade, 1975) and the bronchomotor (Vaage, 1976;Clay & Hughes, 1980) responses to miliary embolism. This could be due to inhibition of either the platelet-release reaction (Cade, 1975;Vaage, 1976) or the release of prostaglandins from lung tissue (Clay & Hughes, 1980).…”

Mechanisms of hypoxemia

“…[55] Bronchoconstriction may be due to the release of substances with bronchoconstriction properties at the sites of thromboemboli, such as acetylcholine, histamine, serotonin, platelet-activating factor, prostaglandins and the plasma kinins leading to reflex bronchoconstriction. [56575859] Pulmonary artery obstruction by thromboemboli also reduces the elimination of CO 2 , leading to reduced alveolar CO 2 tension and hypocapnia-induced bronchoconstriction. [60] Patients with PE may develop surfactant deficiency leading to development of alveolar collapse.…”

Pulmonary vasodilation in acute pulmonary embolism – a systematic review

“…19,49,50 Sympathetic activity seems to be increased in both embolized and non-embolized parts of the lung. 51 PE-released substances also cause bronchoconstriction of the small airways, 23,42,52 leading to hypoxia and pulmonary vasoconstriction. 53 Hypoxia in the lung tissue will inhibit synthesis of vasodilating prostanoids and worsen vasoconstriction.…”